Although vitamin A, which is a naturally-occurring retinoid, is an essential nutrient for normal cellular function, including reproduction and development, there is growing concern that ingestion of excess vitamin A during pregnancy may be associated with birth defects. There is currently inadequate information in humans to designate safe dosages of vitamin A, which is available as a non-prescription supplement. In collaboration with F. Hoffmann-La Roche Ltd., Basel Switzerland, we have examined the dose-response relationship and pharmacokinetics of high doses (20,000 to 80,000 IU/kg/day) of Vitamin A Palmitate administered during early pregnancy (gestational days [GD] 16-27) in the cynomolgus macaque which is a well-established model for the developmental toxicity of several retinoid compounds. Results to date indicate that there is a dose-related increase in teratogenicity following oral administration of 20,000 IU/kg to 80,000 IU/kg vitamin A palmitate. The malformations affected typical retinoid target tissues, including the craniofacial region (hypoplasia of the ear, mandible, zygomatic process, and tympanic ring) as well as the heart (transposition of the great vessels) and thymus (hypoplasia). Since the macaque responds so similarly to the human to retinoid embryopathy, the information derived from these studies has important risk assessment implications. The teratogenic threshold dose of vitamin A in the monkey, which is close to 20,000 IU/kg, far exceeds the recommended level for pregnant women. Although further studies are needed to establish the no observed adverse effect level (NOAEL) in thismodel, these data support the current FDA recommendation of 8,000 IU/day vitamin A supplementation which is the maximum level contained in most prenatal vitamins. *KEY*Teratogenicity, Risk assessment